Researchers: thyroid function depends on what we eat

Editorial Note

The article was previously published in an earlier version, and an updated version is presented here according to scientific and informative criteria. The text is for informational purposes only and does not replace clinical judgment: for personal problems, consult your trusted doctor.

IN BRIEF

• Thyroid function is influenced by metabolic and immunological factors that can be modulated by diet and adiposity status.
• Adipokines (hormones produced by fat) link nutritional status, inflammation, and thyroid regulation; leptin has a historical role, and visfatin is among the most frequently studied adipokines.
• Diets and eating patterns associated with high body weight and insulin resistance show correlations with alterations in thyroid parameters, but the relationship is complex and context-dependent.
• Interventions that reduce weight and inflammation (e.g., weight loss, sleeve/bypass surgery, anti-inflammatory dietary patterns) often report partial normalization of thyroid markers; however, evidence does not support universal prescriptions.

Abstract: What does science say?

The thyroid integrates metabolic, immune, and nutritional signals: the activity of adipose cells (through adipokines) and the individual's metabolic state can modulate the levels and action of thyroid hormones. Observational and experimental studies show associations between obesity, insulin resistance, increased specific adipokines (e.g., visfatin), and alterations in thyroid parameters. Some research suggests that lifestyle and body composition changes can lead to an improvement in hormonal profiles, while direct causal evidence remains limited. Interpretation requires caution: much of the evidence is observational, with heterogeneity in methods, populations, and measurements. Practical guidance for the public is indicative, not therapeutic.

Main Section

What are adipokines and why do they matter for the thyroid?

Adipokines are proteins secreted by adipose tissue that perform hormonal and signaling functions between organs. The discovery of the first gene linked to leptin production in 1994 marked the beginning of the modern understanding of adipose tissue as an endocrine organ, with implications for hunger, metabolism, and energy balance [1]. Subsequent studies have identified numerous adipokines (e.g., adiponectin, resistin, visfatin), some with inflammatory or metabolic properties that can interact with thyroid regulation. A synthetic overview of the experimental and clinical literature on adipokines and the thyroid is available in reviews that integrate clinical data and experimental models, indicating complex relationships between circulating levels of these molecules and thyroid parameters [2].

Visfatin, inflammation, and thyroid function

Visfatin (also known as NAMPT/PBEF) is an example of an adipokine studied for its relationship with inflammation. Analysis of clinical cohorts has shown that blood visfatin levels can be correlated with inflammatory markers independently of insulin resistance [3]. In patients with hyperthyroidism, a reduction in visfatin was found after antithyroid therapy, suggesting that thyroid status can influence the levels of this molecule or vice versa in a way not yet clarified [4]. These results offer biological plausibility for a link between inflammation, metabolism, and thyroid function, but do not establish a direct and generalizable causal relationship for all populations.

Obesity, insulin resistance, and thyroid: observational associations

Numerous epidemiological studies and reviews have identified consistent patterns: obesity is often associated with variations in TSH and free thyroid hormone levels, a phenomenon that can regress after weight loss [5]. The relationship can be bidirectional and mediated by metabolic factors (insulin resistance), inflammatory factors (adipokines), and behavioral factors (diet, physical activity). Recent results suggest that high BMI is also associated, with indirect genetic evidence, with an increased risk of autoimmune thyroid diseases, proposing a possible causal link between adiposity and autoimmune development [6]. However, the transition from association to causality requires more robust longitudinal and intervention studies.

Diet, eating patterns, and thyroid parameters

Surveys of large populations show that dietary patterns characterized by an inflammatory component and richness in refined carbohydrates and ultra-processed foods are associated with worse metabolic profiles and, in some studies, with variations in thyroid levels. A population study highlighted associations between specific cardiometabolic patterns and thyroid parameters measured on a large scale, emphasizing the role of the dietary context in modulating thyroid hormones [7]. However, these analyses are observational and conditioned by confounding factors (dietary iodine, autoimmune status, medications), thus offering indications of plausibility rather than precise clinical recommendations.

Practical Section

What it means in practice

For those seeking practical references, the main message is that thyroid function is integrated into a general metabolic system. Lifestyle patterns that reduce systemic inflammation and promote body weight control are associated with improvements in metabolic parameters that frequently coexist with thyroid alterations. Interventions aimed at weight loss (including surgical procedures in selected cases) are sometimes associated with normalization or improvement of thyroid hormone levels, confirming the plasticity of the system in response to changes in body composition [8].

Which dietary choices have the most evidence?

Evidence does not support a single diet for thyroid health. However, anti-inflammatory dietary patterns rich in unprocessed foods—such as variants of the Mediterranean diet—are associated with lower markers of thyroid autoimmunity and favorable metabolic profiles in multiple observational studies and reviews [9]. It is important to consider the intake of essential micronutrients for hormone synthesis (e.g., iodine, iron, selenium when indicated), but avoiding arbitrary supplementation without clinical supervision.

Physical activity and behavior

Regular physical activity contributes to improved insulin sensitivity, reduced inflammatory markers, and weight management: all factors that can indirectly affect thyroid function. Involvement in exercise programs must be adapted to individual conditions and agreed upon with healthcare professionals when active thyroid diseases or comorbidities are present.

KEY POINTS TO REMEMBER

• The thyroid is influenced by metabolic and immune signals: diet is one of the components that can modulate these signals.
• Adipokines like leptin and visfatin link nutritional status to inflammation and thyroid regulation, but the causal relationship remains complex.
• Obesity is associated with variations in thyroid parameters; weight loss often normalizes some values.
• Anti-inflammatory dietary patterns and correction of nutritional deficiencies are sensible approaches at the population level, but individual choices must be clinically supervised.

Limitations of the evidence

Difference between observational studies and causal evidence: many of the available associations come from observational studies, which test correlations but do not prove causality. Experimental and clinical studies also exist, but are often small or specific to certain populations.

Methodological limitations: heterogeneity in dietary measures, thyroid status assessment (TSH, FT4, FT3, antibodies), considered covariates (iodine, medications, smoking), and follow-up duration makes it difficult to generalize results.

Context variability: results may depend on the local nutritional background (population iodine status), autoimmune status, and age. Prudent interpretation: associations suggest plausible biological hypotheses but require well-designed intervention studies to establish the efficacy and safety of targeted dietary changes.

Editorial Conclusion

The relationship between diet and thyroid function is realistic and multilevel: it includes endocrine signals from adipose tissue, metabolic status, and immune components. The evidence gathered indicates that maintaining an adequate body weight, reducing systemic inflammation, and ensuring correct nutritional intake are strategies consistent with promoting thyroid health at the population level. However, there are no unique solutions: the best path is individual and shared with healthcare professionals. Research continues to explore the mechanisms, and specific clinical trials will be needed to transform some associations into more precise recommendations.

EDITORIAL NOTE

This update integrates knowledge, reviews, and clinical studies available in scientific literature. The article is for informational purposes: it does not constitute medical advice. For diagnoses, therapies, or therapeutic modifications, consult your treating physician.

SCIENTIFIC RESEARCH

1. Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature. 1994;372:425–432. https://doi.org/10.1038/372425a0 [1]
2. Association between novel adipocytokines adiponectin, vaspin, visfatin, and thyroid: an experimental and clinical update. Endocrine Connections. 2013. https://doi.org/10.1530/EC-13-0061 [2]
3. Oki K, Yamane K, Kamei N, Nojima H, Kohno N. Circulating visfatin level is correlated with inflammation, but not with insulin resistance. Clinical Endocrinology (Oxf). 2007;67:796–800. https://doi.org/10.1111/j.1365-2265.2007.02966.x [3]
4. Chu C-H, Lee J-K, Wang M-C, et al. Change of visfatin, C-reactive protein concentrations, and insulin sensitivity in patients with hyperthyroidism. Metabolism. 2008;57(10):1380–1383. https://doi.org/10.1016/j.metabol.2008.05.006 [4]
5. Obesity and thyroid function. Molecular and Cellular Endocrinology. 2009; (review). https://doi.org/10.1016/j.mce.2009.06.005 [5]
6. Cardiometabolic-related dietary patterns and thyroid function: a population-based cross-sectional study. European Journal of Medical Research. 2023; (TLGS analysis). https://doi.org/10.1186/s40001-023-01553-1 [6]
7. Causal association between body mass index and autoimmune thyroiditis: evidence from Mendelian randomization. European Journal of Medical Research. 2023. https://doi.org/10.1186/s40001-023-01480-1 [7]
8. Alterations in thyroid hormones in obese patients are associated with body composition changes after bariatric surgery. The Journal of Clinical Endocrinology & Metabolism. 2024. https://doi.org/10.1210/clinem/dgae605 [8]
9. Autoimmune Thyroid Disorders: The Mediterranean Diet as a Protective Choice. Nutrients. 2023;15(18):3953. https://doi.org/10.3390/nu15183953 [9]